Chapter 10 The Endocrine System The Body’s Other Control System

Chapter 10
The Endocrine System
The Body’s Other Control System
Introduction
The nervous & endocrine system are
totally interconnected & always monitor
each other’s activities.
 Endocrine system also collects information
and sends orders but it is slower, more
subtle control system; while it acts slowly,
effects last longer than those of nervous
system.

Organization of Endocrine System
A series of organs & glands in body that
secrete chemical messengers into blood
stream.
 Exocrine glands, like sweat glands, secrete
out of body, but are not part of endocrine
system that secrete into body.

Hormones
Chemical messengers released by
endocrine glands.
 Released into blood stream & travel all
over body
 Some affecting millions of cells
simultaneously.
 Effects last for minutes, hours or days
 Some, like Insulin, are secreted all the
time, with amount secreted changing PRN.

Hormones con’t
Function by binding to receptors sites on
or inside of target cells.
 Can have several different effects, either
changing cellular permeability or sending
target cell a message that changes
enzyme activity inside cell.

Control of Endocrine Activity
Amount of hormone secreted changes
based on situational demands.
 Many endocrine organs secrete hormones
continuously.
 Many chemical & physical characteristics
of body have standard level, or set-point,
that is ideal level for that particular value.


Examples: BP, Pao2, HR, & blood sugar.
Steroids



Bind to sites inside cells
Lipid molecules that can
pass easily through
target cell membrane,
allowing them to
interact directly with
cell’s DNA to change cell
activity.
Must be carefully
regulated because only
small amounts are
needed.
Negative Feed Back
Endocrine & Nervous system work together
to keep levels at or near homeostasis.
 Example: hypothalamus stores ideal setpoint for temperature.
 If hormone levels rise, negative feedback will
turn off endocrine organ that is secreting
hormone.

Is this Positive or Negative Feed Back?
Positive Feed Back
Increases magnitude of change
 Not a way to regulate body, since positive
feedback increases change away from set
point.

Neural Control
Some hormones are directly controlled by
nervous system.
 When sympathetic nervous system is
active, it sends signals to adrenal glands
to release epinephrine & norepinephrine.
 prolongs effects of sympathetic activity.
 Example:
“fight or flight”
syndrome…


Inspired by Madison
Hormonal Control




Where one gland is controlled by release of
hormones from another gland up the chain
Orders are sent from one organ to another, like a
relay race.
Feedback controls flow of orders via hormones
from one part of chain to the other.
Example:
Hypothalamus
Pituitary
Adrenal
Secretes Cortisol
Humoral Control



A term that pertains to
body fluids or substances.
Directly monitors body’s
internal environment by
monitoring body fluids.
Example: pancreas
secretes insulin in
response to rising blood
glucose levels.
Hypothalamus





Located in “diencephalon”
Link between nervous &
endocrine control systems.
Controls hunger, thirst,
fluid balance, & body
temperature.
Acts as “commander in
chief” for other glands in
endocrine system.
Controls pituitary gland, &
thus, most other glands in
endocrine system.
Pituitary Gland





Part of “diencephalon”
Known as the “master
gland.”
Acts only under orders
from hypothalamus.
If hypothalamus is
“commander in chief,”
pituitary is a high ranking
general.
Split into two segments,
anterior pituitary &
posterior pituitary.
Posterior Pituitary
Extension of hypothalamus
 Secretes ADH (vasopressin): Targets
kidneys/decreases urination when hypothalamus
senses decreased blood volume. ETOH &
caffeine turn off ADH causing dehydration.
 Secretes Oxytocin: maintains uterine
contractions during labor & is involved in
lactation.

Pathology Connection
Diabetes Insipidus
Etiology: under-production of ADH
 S/S: excessive, dilute urine
 RX: fluid & hormone replacement

Microscopic
Hematuria
Normal
Mild Hematuria
Anterior Pituitary
Makes or secretes:
 GH:
Growth Hormone
 TSH:
thyroid-stimulating hormone
 ACTH: adrenocorticotropic hormone
 Prolactin: regulates lactation
 LH:
luteinizing hormone
 FSH:
follicle-stimulating hormone
Go to…
 Table
10-3
Selected hypothalamic & Pituitary
Hormones Chart.
Pathology Connection
Anterior Pituitary
Hypopituitarism
Etiology: decrease in function due to
tumor, trauma, radiation or surgery.
 S/S: vague & subtle
 Dx: imaging & serum hormone levels
 Rx: hormone replacement/tumor removal

Turner’s
Syndrome
Pathology Connection
Anterior Pituitary
Hyperpituitarism




Etiology: overproduction of Pituitary hormones due to
tumor.
S/S:
 Acromegaly
 Reproductive abnormalities
 Cardiac dysfunction
 Sleep apnea
 Cushing’s syndrome
 Hyperthyroidism
Dx: imaging & serum hormone levels
Rx: tumor removal
Pathology Connection
Anterior Pituitary
Cushing’s Syndrome




Etiology: over-secretion of cortisol: Steroids,
pituitary or adrenal tumors, genetic.
S/S: upper body obesity, round face, eccyhmosis,
osteoporosis, fatigue, depression, HTN, &
hyperglycemia. Women excess facial hair &
irregular menses. Men may have decreased
fertility & libido.
Dx: serum analysis, MRI, biopsy
Rx: tumor removal, hormone replacements
Stature Disorders
Dwarfism:
 Etiology: Insufficient GH, genetic
S/S: well-below-average height
 Dx: serum hormone levels
 Rx: hormone replacement injections

Stature Disorders
Gigantism/Acromegaly:
 Etiology: Too much GH.
Anterior Pituitary tumor.
 S/S: In children, rapid growth
to height in great excess of
normal; In adults, excess
growth & deformity of body
tissues.
 Dx: MRI, serum analysis.
 Rx: Tumor removal
Acromegaly
Thyroid Gland
Located in anterior portion of neck & is
butterfly shaped.
 Secretes Triiodothyronine (T3) & Thyroxine
(T4) under pituitary orders; & calcitonin,
involved in calcium storage.
 Contains iodine & control cell metabolism &
growth.

Thyroid Gland con’t
Over or underproduction cause variety of
clinical symptoms.
 Essential in controlling growth &
metabolism of body tissues, particularly in
nervous system.
 Iodine in table salt essential for thyroid
function.

Pathology Connection
Hypothyroidism


Etiology: Either hypothalamus, pituitary, or thyroid
infection, tumor or autoimmune disease.
S/S: Fatigue, feeling cold, dry skin, hair loss,
constipation, bradycardia, leg cramps, weight gain,
hyperlipidemia, hypercholesterolemia, depression,
sexual dysfunction.
Severe Goiter
Mild Goiter
Moderate
Goiter
Hashimoto’s Thyroiditis
Most common cause of hypothyroidism
 Most common in women ages 30-50
Etiology: autoimmune attack on thyroid
S/S: edema, pain, dysphagia
Dx: low serum T4 & elevated TSH
Rx: PO synthetic hormones

Pathology Connection:
Hyperthyroidism- Graves Disease
Etiology: Overproduction of thyroid hormones
S/S: feeling hot, muscle tremors & weakness,
tachycardia, enlarged-bulging eyes, nervousirritable, loose bowels, infertility.
Graves Disease
Most common form of hyperthyroidism
 More common in women of childbearing age
Etiology: autoimmune attack on TSH receptors
of thyroid.
S/S: tremors, sweating, weakness, tachycardia,
arrhythmia, irritability.
Dx: elevated serum T4 & low TSH. MRI
thyroid with radioactive iodine; radioactive
iodine uptake is increased.
Rx: Radiation, thyroidectomy, thyroid
replacement meds.

Parathyroid Glands
2 small pairs of glands embedded in its
posterior surface.
 Produce parathyroid hormone (PTH), which
regulates levels of calcium in blood stream.
 If calcium levels get too low gland releases
PTH, which stimulates bone dissolving cells
& releases calcium into blood.

Thymus Gland
Located in upper thorax-posterior sternum.
 Both endocrine & lymphatic organ
 Produces Thymosin: helps with maturation
of WBCs during childhood to fight infection.
 Begins to hypertrophy during puberty.

Pineal Gland
Tiny gland found within diencephalon of brain.
 Function remains unknown
 Produces hormone melatonin, which rises and
falls during waking & sleeping hours.

Pancreas
Responsible for maintaining BS levels at or near
set-point of 70–105.
 During hyperglycemia pancreas releases insulin
which helps glucose get into cells; excess glucose
affect fluid balance of cells.
 Secretes glucagon, which puts glucose into
bloodstream during hypoglycemia; low glucose
levels affect cell metabolism because all cells
need glucose for cellular respiration.

Control of Blood Glucose by Pancreatic
Hormones
Pathology Connection
Diabetes Mellitus
Abnormal pancreatic hormones
 Hyperglycemia: abnormally high blood glucose
levels.
 2 types of diabetes mellitus:
Type I: Usually Juvenile onset
Type II: Usually Adult onset

Pathology Connection
Type I IDDM
Insulin-dependent diabetes mellitus (IDDM);
juvenile-onset before 40 y/o.
Etiology: Auto-immune destruction of insulin
producing cells of pancreas. inadequate insulin
production.
S/S: usually sudden & severe, urination, extreme
thirst, & weight loss.
Dx: BS, UA
Rx: Insulin replacement via injection, pump, or
pancreas transplant.

Taking Insulin
Pathology Connection
Type II NIDDM
Non-insulin-dependent diabetes mellitus (NIDDM).
 Late or adult onset
Etiology: body tissue insensitivity to insulin, obesity,
sedentary life style.
S/S: more subtle than IDDM Type I
Dx: BS, UA
Rx: Diet/exercise, oral antihyperglycemics, insulin.

Pathology Connection:
Why DM Causes Problems
Hyperglycemia cause kidneys to work
overtime to secrete excess sugar.
 Results in polyuria & polydipsia, renal
damage.
 glucose cannot get into cells to make ATP
 other sources of fuel for ATP production
sought after.
 weight loss as body begins to break down
energy stores of fat & muscle.
 metabolism changes resulting in increasingly
acidic blood.

DM Problems
Difficult wound healing
 Peripheral neuropathy
 Changes in mentation
 Paroxysmal hyper vs hypo glycemia
 Ketoacidosis: break down of fats into ketone
bodies.
 Coma
 Death

Hyperglycemia
Etiology: failure of pancreatic Islets of
Langerhan.
S/S: polyphagia, polyuria, polydipsia, blurred
vision, fatigue, wt loss.
Dx: BS, UA, pt hx
Rx: oral hypoglycemics, insulin, life-style
modifications. Pt/family edu.
Hypoglycemia
Early S/S:
 hunger, nervousness, dizziness, anxiety,
weakness, & difficulty speaking.
Rx:
 STAT replacement of sugar in blood
 Fruit juice, milk, non-diet soda, hard candy, then
a regular meal.
Later S/S:
 mental confusion, seizures, coma & possibly
death
Rx: STAT medical attention: Glucagon, IV glucose,
food when alert & stable.
Body’s defense against Hypoglycemia
Multiple organs attempt to correct BS deficit
 Pancreas: decreases insulin secretion, increases
glucagon secretion.
 Adrenal Glands: sympathetic nervous system
triggers release of epinephrine.
 Hypothalamus: triggers feelings of hunger, so
patient will eat food.
Go to…
 Table
10-4
Comparison of Type I & Type II
Diabetes chart.
Adrenal Glands
Pair of small glands that sit on kidneys, like
baseball hats.
 Split into 2 Regions
 Adrenal cortex is outer layer
 Adrenal medulla is middle of the gland

Adrenal Medulla
Releases two hormones
 Epinephrine (adrenalin)
 Norepinephrine (both hormone &
neurotransmitter).
 Increase duration of effects of sympathetic
nervous system; effects of hormones last
longer than neurotransmitter.
 Effects include increased HR, BP, &
respiration, diaphoresis & dry mouth.
Adrenal Cortex
Releases Adrenocorticosteroids under
direct stimulation of anterior pituitary.
 decrease in production could be fatal
relatively quickly (Addisonian crisis).
 Regulates fluids, electrolytes, BS,
reproduction, secondary sexual
characteristics, cell metabolism, growth, &
immune system function.

Addison’s Disease
Etiology: adrenalcorticosteroids deficiency due
to autoimmune attack on adrenal cortex,
cancer or infection.
S/S Mild: weakness, fatigue, hypoglycemia,
depression.
Dx: imaging & blood tests for corticosteroids
Rx Mild: hormone replacement
S/S Crisis: acute hypotension, acute
hypoglycemia, acidosis, coma.
Rx Crisis: IV steroids, IV NS, IV Dextrose, IV
Na HCO3, O2, cardiac monitoring.
Therapeutic Steroids
Prednisone used in treatment of
inflammation, organ rejection, immune
disorders.
 can have dangerous side effects including

 Bone
loss
 Weight gain
 Hair growth
 Fat deposits
 Delayed wound healing
 Caution: Do not stop steroids suddenly!
Decrease over time only!!!
Illegal Anabolic Steroids
Causes large increase in muscle mass
 Used to enhance performance or muscle size.
Side Effects Men:
 Atrophy of testicles and decreased sperm
production.
 enlarged breasts
Side Effects Women:
 deepening of voice
 decreased breast size
 excessive body hair growth(yuck!!)

Anabolic Side Effects both Genders
Increased cholesterol levels
 Cardiovascular disease
 Weakened immune function
 exposure to hepatitis B or HIV through
sharing needles.
 Aggressive behavior
 Note: steroids are banned by all major
professional & amateur athletic
organizations.

Anabolic Side Effects
Cortisol & normal stress response
Sympathetic nervous system activates
 Stimulates Adrenal glands
 Epinephrine & norepinephrine: raise BP,
HR, respiration rate & BS; decreases
digestion & other less urgent physiological
functions.
 Cortisol increases blood sugar; changes
immune response.
 prepares body to rapidly expend energy,
beneficial in short term.

Cortisol & Chronic stress response
Chronic Cortisol secretion can result in:
 Increased appetite
 increase autoimmunity and decrease
defense against infection.
 increased HR, HTN, hyperglycemia,
hypercholesterolemia, abdominal fat,
anxiety, depression.
Gonads




Greek for seed
include testes & ovaries
function to produce & store gametes:
Eggs & Sperm.
Produce sex hormones which control
reproduction: Testosterone in men &
Estrogen in women.